We propose that meaningful correlations exist between: 1) the documented deregulation of feedback control over cholesterol biosynthesis in hepatomas, 2) the resulting endogenous enrichment of cell and organelle membranes with cholesterol and its esters, and 3) the potential alterations in the kinetic parameters of anion transport in tumor mitochondria. We are focusing attention on two critically important exchange transport processes in mitochondria; citrate and adenine nucleotide (ADP/ATP) transport. Transport kinetics will be studied by inhibitor-stop methods employing the specific transport inhibitors 1,2,3-denzenetricarboxylate (citrate) and carboxyatractyloside (adenine nucleotide). We shall investigate whether or not an observed rise (or other kinetic alteration) in citrate and ADP/ATP transport efficiency (Vmax, Vinitial, Km) occurs in two lines of Morris hepatoma, 3924A and 16, their hosts, and normal (control) mitochondria. We will correlate any changes noted in the transport kinetics with endogenous levels of cholesterol in the mitochondrial membranes of hepatomas. We will learn whether enrichment of the mitochondrial inner membrane with cholesterol constitutes a sufficient alteration in composition to effect both qualitative and quantitative shifts in citrate and ADP/ATP transport characteristics. This last question will be approached via a new method we have developed which permits the rapid transfer of cholesterol into the membranes of normal mitochondria in vitro, resulting in their becoming sterol-rich.